The actions of saralasin on the renal circulation of man and dog; evidence for a sympathetic neural component to vasoconstriction.
The mechanism of renal vasoconstriction produced by saralasin and its dependence on the sympathetic nervous system was investigated in subjects with mild essential hypertension and in anaesthetized dogs. Fluid or saline was given to maximize agonist vasoconstrictor responses. The changes in renal haemodynamics produced by intravenously infused saralasin (dose 0.01-10 microgram kg-1 min-1) were assessed by clearance methods. In the patients, it induced a dose-related renal vasoconstriction which correlated with a rise in plasma noradrenaline levels. In dogs with innervated kidneys it also caused vasoconstriction. But in dogs with denervated kidneys it caused vasodilatation. Infusion at the highest dose directly into the renal artery of denervated kidneys induced only vasodilatation. We conclude that one component of the renal vasoconstriction that occurs with intravenous saralasin infusions is mediated by the renal nerves.
D000328:Adult; D000804:Angiotensin II / Q000031:analogs & derivatives*; D000818:Animals; D003714:Denervation; D004285:Dogs; D005260:Female; D006801:Humans; D007668:Kidney / Q000098:blood supply* / Q000294:innervation; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow / Q000187:drug effects; D012504:Saralasin / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects
D000804:Angiotensin II; D012504:Saralasin